Obesity is associated with several health conditions, the most devastating of which is type 2 diabetes. Obesity occurs when energy intake exceeds energy expenditure. Current weight loss therapies targeting the reduction of food intake have proven to be relatively ineffective, and the ability to reduce the risk of obesity-related complications is limited. Energy balance is controlled by a brain region called hypothalamus, whose neuronal inputs and outputs are also critical in the regulation of glucose homeostasis.

Our primary research focus is the neuroendocrine regulation of food intake, energy homeostasis and glucose metabolism, with a special emphasis on evaluating the critical actions of centrally- and peripherally-produced NPY, PYY and PP in these processes, including the molecular mechanisms and neuronal pathways underlying these actions by using germline and conditional transgenic and knockout mouse models available and molecular techniques. More recently, we have been particularly active in elucidating the role of neuropeptide Y family including PYY and their receptors in the control of insulin synthesis and secretion as well as glucose metabolism through direct neural signalling and modulation of local endocrine function. In addition we have been interested in examining the important interplay between adipose tissue and bone.

Our recent work has identified critical brain circuits that could explain the clinical phenomenon that the harder some obese people diet, the harder it is for them to lose weight. Our novel research findings have contributed to a better understanding of these fundamental processes with potential to develop therapeutical targets for the treatment of obesity and its most ominous complication, diabetes.